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Pharm Res. 2012 Jun;29(6):1506-17. doi: 10.1007/s11095-011-0625-0. Epub 2011 Dec 3.

Apigenin attenuates insulin-like growth factor-I signaling in an autochthonous mouse prostate cancer model.

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1
Department of Urology, Case Western Reserve University, 2109 Adelbert Road, Wood Research Tower, RTG01, Cleveland, Ohio 44106, USA.

Abstract

PURPOSE:

Deregulation of IGF signaling plays an important role in prostate cancer and contributes to invasion and metastasis. We determined the effect of apigenin, a plant flavone, on IGF signaling and its downstream targets in TRAMP mice.

METHODS:

Mice received p.o. apigenin at 20 and 50 μg/day dose for 20 weeks. ELISA, Western blotting and immunohistochemistry were performed to examine the IGF-axis and its regulated pathway in response to apigenin intake.

RESULTS:

Increased serum levels of IGF-I, VEGF, uPA and concomitant decrease in IGFBP-3 were observed; p-Akt (Ser473), p-ERK1 (T202/Y204) and p-ERK2 (T185/Y187) expression increased in the dorso-lateral prostate of TRAMP mice during the course of cancer progression as a function of age. P.o. administration of apigenin resulted in substantial reduction in the levels of IGF-I and increase in the levels of IGFBP-3 in the serum and the dorso-lateral prostate. This modulation of IGF/IGFBP-3 was associated with an inhibition of p-Akt and p-ERK1/2. Apigenin intake resulted in marked inhibition of VEGF, uPA, MMP-2 and MMP-9 which coincided with tumor growth inhibition and complete absence of metastasis in TRAMP mice.

CONCLUSIONS:

Our results indicate that apigenin effectively suppressed prostate cancer progression in TRAMP mice by attenuating IGF-I/IGFBP-3 signaling and inhibiting angiogenesis and metastasis.

PMID:
22139534
PMCID:
PMC4017263
DOI:
10.1007/s11095-011-0625-0
[Indexed for MEDLINE]
Free PMC Article

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